Parkinson's disease (PD) is a chronic, progressive, neurodegenerative disorder, which occurs as a result of the loss of dopaminergic neurons in the brain, but whose cause is unknown. PD was first written about by English physician, James Parkinson in 1817. He described the illness in an essay titled ‘The Shaking Palsy’, as an “involuntary tremulous motion, with lessened muscular power, in parts not in action even when supported, with a propensity to bend the trunk forward and to pass from a walking to a running pace”. This statement described many of the features that are associated with PD today.
The onset of PD is very gradual and many patients cannot remember when their symptoms began. The early symptoms of PD are often vague and non-specific, and amongst many other symptoms often include tiredness, fatigue, weariness, muscle aches, and cramps. There are three cardinal motor features of PD; these are tremor, rigidity and bradykinesia.
In literature, bradykinesia, akinesia and hypokinesia are commonly confused. Bradykinesia is defined as a slowness of ongoing movement, whereas akinesia is failure to initiate a willed movement, and hypokinesia is the reduction of movement. It is not known if these features are related, although one study evaluated the relation between bradykinesia and hypokinesia and concluded a lack of relation between the two features. This means that in literature ‘bradykinesia’ is often used to encompass many different aspects of poverty of movement; including prolonged reaction time to initiate a movement, prolonged time to discontinue a false movement, prolonged time to change a motor pattern, rapid fatigue on long tasks and slow execution of movement (see e.g van Hilten, J., et al., “Bradykinesia and hypokinesia in Parkinson's disease: What's in a Name?”, Journal of Neural Transmission, Vol. 105, 1998, pp. 229-237). Several proposals have been offered as explanations for why PD subjects move more slowly than normal subjects, although a single mechanism has not been achieved. These proposals include suggestions that bradykinesia results from a lower production of force, that PD subjects adopt a behavioural strategy of moving slowly in order to maintain their accuracy, and that bradykinesia may result from a basic defect in ability to internally organise motor output (Majsak, M., et al., “The reaching movements of patients with Parkinson's disease under self-determined maximal speed and visually cued conditions”, Brain, Vol. 121, 1998, pp. 755-766).
A Berrardelli, et al. (“Pathophysiology of bradykinesia in Parkinson's disease”, Brain, Vol. 124, 2001, pp. 2131-2146) have considered five factors that contribute to bradykinesia. These are:    i. muscle weakness, which is likely to contribute to slowness of movement in some muscle groups;    ii. rigidity, which may lead to slower reflexes;    iii. tremor, which may be a factor in prolonging reaction times and the persistence of action tremor may lead to muscle weakness;    iv. movement variability, whereby PD subject's movements are less accurate than normal subjects, particularly when they have to move quickly; and    v. slowness of thought (bradyphrenia), which could interfere with movement planning and increase movement time.
Bradykinesia is commonly observed in patients as facial immobility (hypomimia), infrequent blinking, paucity of normal gesture and lack of expression, as well as sudden stopping of ongoing motion, known as ‘freezing’. Bradykinesia is thought to be present in 77-98% of cases of PD; however it also occurs in many other related disorders (including progressive supranuclear palsy, multiple system atrophy, Alzheimer's disease and depression) and is also common in old age (“Pathophysiology of bradykinesia in Parkinson's disease”, Brain, Vol. 124, 2001, pp. 2131-2146).
There are many other features that are related to PD, apart from the cardinal symptoms described above. Other features include: reduced arm swing on walking, stooped posture with shuffling gait, falls; micrographia (small and illegible handwriting), due to the clumsiness of hand movements and difficulty with fine motor tasks, Parkinsonian dysarthria (speech disorders). These are estimated to be present in more than 75% of PD patients and may consist of reduced loudness, monotone, imprecise articulation, and/or disordered rate, Dysphagia (difficulty in swallowing) which may lead to drooling of saliva and poor nutritional status, bradyphrenia (slowness of thought), depression which is estimated to be present in 40-50% of patients, cognitive problems and dementia which are estimated to be present in 48-80% of patients, olfactory dysfunction (lack of sense of smell) which is thought to affect 70% of patients and sleep disorders.
The term ‘Parkinsonism’ refers to any condition which shows the common motor symptoms of PD (tremor, rigidity and bradykinesia), therefore some patients with Parkinsonism do not have idiopathic Parkinson's disease (referred to in this study simply as Parkinson's Disease). PD is the most common cause of these symptoms, however a study of patients with Parkinsonism found that 65% had PD, 18% had drug-induced Parkinsonism, 7% had vascular Parkinsonism (caused by blockages in the small blood vessels feeding the brain) and 10% had atypical Parkinsonism. The most common atypical Parkinsonism syndromes are multiple system atrophy (MSA) and progressive supranuclear palsy (PSP), but also include diffuse Lewy body disease, corticobasal degeneration and overexposure to certain substances (e.g. manganese and MPTP).
Thus, bradykinesia is an important element in the diagnosis of a disease or responses to drugs or toxins. Although having a central role in the diagnostic armoury, the identification of the presence of bradykinesia is not itself a diagnosis of any particular clinical condition.
The tapping test is used routinely for the quantification of drug effects on motor slowness in PD and is described below.
Many different types of equipment have been used to measure the tap rate of PD patients, including: electronic touchpads with touch plates (Muir, S., et al., “Measurement and Analysis of Single and Multiple Finger Tapping in Normal and Parkinsonian Subjects”, Parkinsonism & Related Disorders, Vol. 1, No. 2, 1995, pp. 89-96); a computer keyboard (Giovanni, G. et al., “Bradykinesia akinesia inco-ordination test (BRAIN TEST): an objective computerised assessment of upper limb motor function”, J Neurol Neurosurg Psychiatry, Vol. 67, 1999, pp. 624-629), computer-interfaced musical keyboards (Tavares, A., et al., “Quantative Measurements of Alternating Finger Tapping in Parkinson's Disease Correlate With UPDRS Motor Disability and Reveal the Improvement in Fine Motor Control From Medication and Deep Brain Stimulation”, Movement Disorders, Vol. 20, No. 10, pp. 1286-1298, 2005), buttons (interfacing a microcomputer) and accelerometers (Dunnewold, R., Jacobi, C. & van Hilten, J., “Quantitative assessment of bradykinesia in patients with Parkinson's disease”, Journal of Neuroscience Methods, Vol. 74, 1997, pp. 107-112).
All of the studies described above found that PD patients had a significantly lower tap rate than normal control subjects. Many studies have found that the tap rate correlates well with ratings given from the motor sections of the UPDRS scale.
R. Dunnewold, et al. measured the movement time of subjects along with the tapping score. The movement time used in this study was calculated as the time for a subject to react to visual stimuli on a video display. It was found that a correlation above 0.75 was found between the tapping rate and the movement time of the subjects, however low correlations were found between the score from the motor section of the UPDRS scale and the tap rate and movement time. Many other studies have also considered reaction time (time from the ‘go’ signal until the onset of movement) and movement time (time between movement onset and reaching target) of subjects in response to various stimuli. Movement time is the physiologic correlate of bradykinesia, and reaction time is the correlate of akinesia. These studies discovered that PD patients exhibit a significantly prolonged reaction time compared to controls.
R. Watts, et al. (“Electrophysiologic analysis of early Parkinson's disease”, Neurology, Vol. 41, Supplement 2, 1991) used a simple touchpad with a ‘start’ location and two ‘target’ locations to measure reaction time. Two tasks were used; the first where the target location was specified before the ‘go’ signal was given, and a second where the target location was shown on the ‘go’ signal. It was found that reaction time was prolonged in PD patients compared to controls where the target location was predefined, but not where the subjects had to choose the target on the ‘go’ signal. Movement time was found to be prolonged in both tasks for PD subjects compared to controls.
M. Zappia, et al. (Zappia, M., et al., “Usefulness of movement time in the assessment of Parkinson's disease”, J Neurol, Vol. 241, 1994, pp. 543-550) compared movement time and reaction time, before and after Levodopa administration. It was found that off treatment, movement time and reaction time of the most affected side were significantly related to the severity of PD. After Levodopa administration the movement time improvement related to the severity of PD, whereas reaction time did not.
M. Hallett and S. Khoshbin (“A Physiological Mechanism of Bradykinesia”, Brain, Vol. 103, 1980, pp. 301-314) carried out a study in 1980 into rapid elbow movements of the dominant arm in PD patients and controls. The subjects were seated in a chair with their arm strapped to a splint with a potentiometer incorporated into the hinge, which was able to convert the rotation of the elbow into a variable voltage. The subjects made fast, accurate elbow flexion movements, beginning at 120°, moving to 80°, 100° and 110°. It was found that normal subjects made all of these movements in the same amount of time with a single ‘triphasic’ pattern of successive bursts of the bicep, tricep and bicep muscles. Most PD patients exhibited alternate bursts longer than the three bursts of activity seen in the controls (up to twelve bursts), which tended to occur more for the longer movements. This is thought to represent a physiological mechanism of bradykinesia.
K. Maitra and A. Dasgupta (“Usefulness of movement time in the assessment of Parkinson's disease”, J Neurol, Vol. 241, 1994, pp. 543-550) performed a study using fast reach-to-grasp movements without any visual stimuli in PD patients. Movement of the subject's upper arm (measure of reach) and movement of the index finger (measure of grasp) were recorded using magnetic trackers. The experiment was conducted in a dimly lit room, where subjects stood with their upper arm by the side of their body and on the command of ‘go’, performed a fast reaching and grasping movement without any physical object to grasp. It was found that the controls performed each movement rapidly with a smooth single peak velocity with near symmetrical acceleration and deceleration phases. The angular movements were found to have minimal variability under repetitive trials. The PD patients however, moved much slower with less amplitude and greater variability over repeated trials. The total movement in PD patients seemed to be sequential, rather than continuous as seen in the control patients. It was concluded that bradykinesia in participants with PD resulted from a defect in switching from one motor programme to another.
The tapping test is used routinely for the quantification of drug effects on motor slowness in PD, and many different types of equipment have been used to measure the tap rate of PD patients in previous studies. A number of studies have also considered reaction time and movement time of subjects in response to a stimulus. Bradykinesia is measured in the UPDRS scale by asking patients to perform finger taps, hand movements and rapid alternating movements of hands, in both the left and right hands. The tasks used to measure bradykinesia in the UPDRS scale are shown below:
The tapping test is commonly performed by subjects tapping their thumb with their index finger as many times as possible in 30 seconds for each hand.
The tasks chosen to observing resting tremor and bradykinesia in this study were both hand-based, so collection of the most useful data was obtained by attaching the sensors to the hands of the participating subjects. As the tapping test involved the thumb and index finger of the subjects, sensors for the bradykinesia task were attached on the thumb and index finger. During the tapping test most movement of the fingers occurs at the end of the digits, therefore it was decided that one of the sensors would be placed on the nail of the subject's thumb and the other sensor on the nail of the subject's index finger.
However there are no reliable techniques for the detection of bradykinesia, therefore the inventors have employed novel computing techniques for the detection of bradykinesia.